The effects of intense light exposure in normal and retinal dystrophic rats will be determined by measuring light induced changes in the rod outer segment (ROS) and retinal pigment epithelium (RPE) membrane lipids and proteins. To this end, collaborative arrangements have been made to measure opsin by radioimmunoassay in ROS from light exposed eyes and to acquire RPE cells grown in tissue culture from normal and dystrophic rats. Current hypotheses of ocular light damage will be investigated by correlating the rhodopsin content in retinas of rats fo various ages and light rearing histories to the concentrations of hydroperoxides and the ascorbic acid content, which are known to be altered during intense light exposure. Both biochemical and histological evidence will be gathered to substantiate the extent of visual cell death in the light exposed eyes of rats. The variables duration of exposure, light intensity and intermittant short light-dark cycles will be investigated as they relate to the sequence of ocular tissue destruction in the retina and RPE and as they relate to the exquisite sensitivity of young dystrophic rats to light. Studies of retinal lipid metabolism will be performed to assess the ability of the photoreceptor cell to repair its membranes during light exposure and to gain insites into the molecular sequence of light damage. A mechanistic study of ROS peroxidative membrane destruction is planned by comparisons of the in vivo process with that which occurs during in vitro incubation in light. The prophylactic effects of young age, cyclic light rearing and vitamin A deficiency will be studied as they relate to visual cell loss from light and in the development of strategies to prevent that process in experimental animals. These studies should lead to a better understanding of retina-RPE interactions during light exposure and have implications in the assessment of ocular light damage in humans from intense monochromatic light sources. The extension of these studies to the genetically blind retinal dystrophic rat has implication, by extrapolation, to human retinal abnormalities of a genetic nature.